In the evaluation of heart signals expressed through vectors in time and space, a significant role belongs to electrode positioning 100 on arbitrarily agreed precise locations, as shown in FIG. 1. Depending on the type of electrocardiogram (“EKG”) recorder, Einthoven bipolar leads D1, D2, and D3 with Baily triaxial system of amplification are in use: aVR, aVL, and aVF (which essentially do not change merits in mathematical sense), so that an EKG inscription is being read from different angle perspectives in 6 xtremity leads of 60 degrees angles, as shown in FIG. 2. An additional 6 leads, VI, V2, V3, V4, V5 and V6, are obtained from a unipolar recording system for measuring, as shown in FIG. 3.
An EKG of a healthy person includes the P wave, QRS complex (including Q, R and S waves) and T wave, as shown in FIG. 4. The real waves are the P wave and the T wave. They can be positive, negative or biphasic. A Q wave is negative, an R wave is positive, and the S wave is negative. Specific wave type is determined on the basis of the R wave location in the following manner if a negative wave precedes the positive R wave then it is the Q wave. If a negative wave follows after R wave, then it is an S wave. Otherwise, in a normal QRS complex, there is no more than one positive wave (i.e., the R wave). If other R waves exist, as it is generally in pathological states, they are denoted R. If there is only one negative wave, without the positive R wave, then it is not clear whether it is the S or the Q wave, so it is called a QS wave or complex.
Fast and large changes in the size and direction of total dipole that are generated during ventricular depolarization result in a QRS complex seen on an EKG. A normal process is shown in FIG. 5. The start of ventricular depolarization usually happens on the left side of the medial part of interventricular septum. Analysis of heart dipole which is further generated by initial depolarization, with an aid of Einthoven's triangle, shows that this dipole has negative a component on lead I, a small negative component on lead II and a positive component on lead III. On FIG. 5, one may spot how dipoles make opposite deflection in individual leads. For example, the Q wave appears in leads I and II, but not in lead III. The second row in this picture shows both ventricles during instantaneous ventricular depolarization in the moment of the largest number of total dipole with the most similar orientation. This phase creates a large total dipole, which is responsible for the R wave on an EKG. Such a dipole is almost parallel with lead II.
As it is shown, such dipole creates a big positive R wave on all three leads. The third row in FIG. 5 shows a situation at the end of a depolarizing spread through chambers and shows how a small total dipole is at that very instant in the S wave creation. The S wave is not necessarily present in all leads. The bottom line shows that during ST segment formation, all cells within both chambers are in a depolarized state. There is no wave of electrical activity that is transmitted through the heart tissue. There is no total dipole (i.e. difference between two body surface points regarding electrical potential). An EKG record is flat at that point, i.e. isoelectrical.
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (“ARVD/C”) is a genetic disorder which is associated with concealed involvement of the right chamber (“RV”) and its structural and functional changes (which are the result of such replacement of heart tissue with fat and fibrous tissue), and electrical insta-bility causes ventricular arrhythmias and sudden cardiac death (“SCD”). Sudden cardiac death is a natural death caused by problems with the heart preceded by loss of consciousness, which lasts about an hour and is a consequence of the acute heart problems. Sudden cardiac death often occurs in people who are generally healthy. Those who die a sudden death, probably are never aware of the potential risk they carry. Frequency of sudden cardiac death with unknown cause is estimated to be between 1/2000 people to 7/1000 people and can af-fect any age, sex, geographic or socioeconomic position. SCD is somewhat less common in USA than in Europe. In Europe, SCD is somewhat more frequent in the Mediterranean region, than in the northern part of Europe, due to population migrations through history. Endemic regions are Veneto in northern Italy with 80% of incidence and island Naxos in Greece with 50% of incidence.
Noninvasive and invasive methods for evaluation of the shape and function of the RV have inherent limitations, due to the complex construction of its shape. Examination of the RV could be a difficult task for a clinical doctor, considering its geometric complexity and that it is divided into three parts: in-flow, outflow and an RV body, which is falciform and abbreviated. The free wall of the RV may have more or less trabeculations, which in combination to its ret-rosternal position limit precise chamber measuring and determination of wall thickness. Tricuspid anterio-postrior systolic excursion (“TAPSE”) has been shown to correlate well with global function (in adult population) as ejectional fraction of left ventricle (“EF LV”) whereas objectively assessed by radionuclide ventriculography (done by standard way). Recognizing mild, frusta, or localized forms, remains a clinical challenge. It is difficult to diagnose ARVD/C in a patient with minimal involvement of the RV on heart ultrasound or contrast angiography. So far, only “V sign” on heart ultrasound has been attributed as pathognomonic. The recommended criteria for ARVD/C early phase detection from World Health Organization (and its working group on ARVD/C) have been found insufficient for this matter. The early identification of sport players who carry genes for ARVD/C plays a central role in the prevention of SCD during sports activities. Most frequent clinical manifestations of the disease are depolarize-repolarize changes on EKG, mainly localized in right precordial leads, global regional morphologic or functional changes of the RV and arrhythmias coming from the RV. Even an asymptomatic person can be diagnosed based on a positive EKG change and ventricular arrhythmia.
An EKG record has technical restrictions in diagnostic span with respect to the analysis of an aggregate value of vector trajectories in each instant of propagation of the electrical heart dipoles. Conversely, a vectorcardiogram (“VCG”) record is an attempt for objectification of relativity of differences in potential in standard EKG devices to maximize its diagnostic capacity. In other words, vector cardiogram represents a “tridimensional electrocardiogram”.
The vectorcardiographic appearance of an EKG represents a stereo metric loop (i.e., a closed curve or trajectory), which is usually shown in separate planes defined by an appropriate axis (frontal: X,Y), (sagittal: Y,Z) and (horizontal: X,Z), as shown in FIG. 6. However, not all signal value is seen from the aspect of separate two-dimensional planes, but it is necessary to observe the loop in three-dimensions. This offers the maximum usability of an analyzed signal in diagnostic and therapeutic sense, because vectorcardiography overcomes imperfections of a typical EKG approach and provides a view of a larger real picture, as shown in FIG. 7.
The reason for this is that every moment some part of atrial or ventricular heart muscle produces a small amount of the electrical force, directed up or down, right or left; and since the heart is a tridimensional structure, the electrical force also moves forwards or backwards. Spatially oriented electrical forces which are generated by the heart appear in a certain order, but not simultaneously.
The form and magnitude of the P wave, QRS complex, ST segment and T wave are set by management direction of aggregate vector and separate vector resultants determined by the location of unipolar precordial leads. A central direction of a depolarization process reflects the sum of all vectors in each part of ventricular myocardium.